Pub Date : 2017-04-07DOI: 10.4172/2168-975X.1000229
Venkateswaran Rajagopalan, Zhi-guo Jiang, G. Yue, Jelena Stojanovic-Radic, E. Pioro, G. Wylie, and Abhijit Das
Diffusion tensor imaging (DTI) is one of the most powerful magnetic resonance imaging (MRI) techniques developed in the twentieth century. In spite of the fact that DTI has been in use for more than two decades, it is still hard to find publications that simplify mathematics behind DTI for DTI users without extensive mathematical background. We believe that this may prevent some researchers from using DTI technique to its fullest extent. To the best of our knowledge, there are no published reviews which have tried to clarify the methods of DTI measurement and analysis. In this article, we attempted to explain the mathematics of DTI in simple terms with the goal of providing DTI users, with a better understanding of this technique and its usage. In addition, we have also described the DTI processing steps and explained the reasons behind each step.
{"title":"A Basic Introduction to Diffusion Tensor Imaging Mathematics and ImageProcessing Steps","authors":"Venkateswaran Rajagopalan, Zhi-guo Jiang, G. Yue, Jelena Stojanovic-Radic, E. Pioro, G. Wylie, and Abhijit Das","doi":"10.4172/2168-975X.1000229","DOIUrl":"https://doi.org/10.4172/2168-975X.1000229","url":null,"abstract":"Diffusion tensor imaging (DTI) is one of the most powerful magnetic resonance imaging (MRI) techniques developed in the twentieth century. In spite of the fact that DTI has been in use for more than two decades, it is still hard to find publications that simplify mathematics behind DTI for DTI users without extensive mathematical background. We believe that this may prevent some researchers from using DTI technique to its fullest extent. To the best of our knowledge, there are no published reviews which have tried to clarify the methods of DTI measurement and analysis. In this article, we attempted to explain the mathematics of DTI in simple terms with the goal of providing DTI users, with a better understanding of this technique and its usage. In addition, we have also described the DTI processing steps and explained the reasons behind each step.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72636895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-13DOI: 10.4172/2168-975X.1000227
Yutian Yu, Xiao Guo, Guangxia Chen, Shaoyuan Li, P. Rong
Insomnia disorder is causing great economic burden to the society. Conventional pharmacotherapies are with multiple adverse effects to people. Auricular acupuncture (AA) inspired us to invent transcutaneous auricular vagus nerve stimulation (taVNS) years ago. We accidently found that taVNS could improve patients sleeping conditions in depressed and in epilepsy patients. And, taVNS is with little side effect. We considered that taVNS is a promising alternative therapy for insomnia disorder with a bright future.
{"title":"Transcutaneous Auricular Vague Nerve Stimulation: A PromisingAlternative Therapy for Insomnia Disorder","authors":"Yutian Yu, Xiao Guo, Guangxia Chen, Shaoyuan Li, P. Rong","doi":"10.4172/2168-975X.1000227","DOIUrl":"https://doi.org/10.4172/2168-975X.1000227","url":null,"abstract":"Insomnia disorder is causing great economic burden to the society. Conventional pharmacotherapies are with multiple adverse effects to people. Auricular acupuncture (AA) inspired us to invent transcutaneous auricular vagus nerve stimulation (taVNS) years ago. We accidently found that taVNS could improve patients sleeping conditions in depressed and in epilepsy patients. And, taVNS is with little side effect. We considered that taVNS is a promising alternative therapy for insomnia disorder with a bright future.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77909566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-13DOI: 10.4172/2168-975X.1000228
H. Al-Jehani, Faisal Alabbas
The development of brain arteriovenous malformations (AVMs) remains enigmatic. Their usual presentation with hemorrhage could be a devastating event. Their second mode of presentation; Seizure poses a mechanistic, diagnostic and therapeutic challenge. For the most part, vascular development and flow abnormalities are implicated in the development of seizures in the context of brain AVMs. Proposed is a hypothesis in which common cortical and vascular development pathways lead to perturbation of the vascular phenotype resulting in arteriovenous shunting while simultaneously leading to focal form of cortical dysplasia conducive of seizure.
{"title":"Epilepsy and Intracranial Vascular Malformations: A Possible MissingLink!","authors":"H. Al-Jehani, Faisal Alabbas","doi":"10.4172/2168-975X.1000228","DOIUrl":"https://doi.org/10.4172/2168-975X.1000228","url":null,"abstract":"The development of brain arteriovenous malformations (AVMs) remains enigmatic. Their usual presentation with hemorrhage could be a devastating event. Their second mode of presentation; Seizure poses a mechanistic, diagnostic and therapeutic challenge. For the most part, vascular development and flow abnormalities are implicated in the development of seizures in the context of brain AVMs. Proposed is a hypothesis in which common cortical and vascular development pathways lead to perturbation of the vascular phenotype resulting in arteriovenous shunting while simultaneously leading to focal form of cortical dysplasia conducive of seizure.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81158726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01DOI: 10.4172/2168-975X.1000239
N. Camara, Emmanuel Binyet
The aim of this paper is to increase awareness of the prevalence of neurological disorders. To do so, we highlight via in-depth literature review the distinction between mental disorders, brain diseases and psychiatric disorders. This distinction will give a holistic view into the disorders. This in turn will facilitate the suggestion of reasonable conclusions that can enhance the way in which mental disorders or brain diseases are being diagnosed and treated.
{"title":"Are Mental Disorders Brain Diseases and What Does This Mean","authors":"N. Camara, Emmanuel Binyet","doi":"10.4172/2168-975X.1000239","DOIUrl":"https://doi.org/10.4172/2168-975X.1000239","url":null,"abstract":"The aim of this paper is to increase awareness of the prevalence of neurological disorders. To do so, we highlight via in-depth literature review the distinction between mental disorders, brain diseases and psychiatric disorders. This distinction will give a holistic view into the disorders. This in turn will facilitate the suggestion of reasonable conclusions that can enhance the way in which mental disorders or brain diseases are being diagnosed and treated.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84506124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01DOI: 10.4172/2168-975X.1000241
A. Ali
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that leads to memory loss and nerve cell death throughout the brain. It is the most common cause of dementia and represents the most important problem in elderly. Dementia characterized mainly by decline in memory, cognitive skills and ability to perform everyday activities as well as behavioral dysfunction. The decline occurs because neurons involved in cognitive function have been destroyed and affected other parts of the brain involved in different basic bodily functions.
{"title":"Risk Factors in Induction and Progression of AlzheimerâÂÂs Disease: Impacton Protection and Disease-Modifying Factors","authors":"A. Ali","doi":"10.4172/2168-975X.1000241","DOIUrl":"https://doi.org/10.4172/2168-975X.1000241","url":null,"abstract":"Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that leads to memory loss and nerve cell death throughout the brain. It is the most common cause of dementia and represents the most important problem in elderly. Dementia characterized mainly by decline in memory, cognitive skills and ability to perform everyday activities as well as behavioral dysfunction. The decline occurs because neurons involved in cognitive function have been destroyed and affected other parts of the brain involved in different basic bodily functions.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82816687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01Epub Date: 2017-05-01DOI: 10.4172/2168-975X.1000232
Jyotshna Kanungo
The pathogenesis of Alzheimer's disease (AD), characterized by prevalent neuronal death and extracellular deposit of amyloid plaques, is poorly understood. DNA lesions downstream of reduced DNA repair ability have been reported in AD brains. Neurons predominantly use a mechanism to repair double-strand DNA breaks (DSB), which is non-homologous end joining (NHEJ). NHEJ requires DNA-dependent protein kinase (DNA-PK) activity. DNA-PK is a holoenzyme comprising the p460 kD catalytic subunit (DNA-PKcs) and its activator Ku, a heterodimer of p86 and p70 subunits. Ku first binds and then recruits DNA-PKcs to double-stranded DNA ends before NHEJ process begins. Studies have shown reduced NHEJ activity as well as DNA-PKcs and Ku protein levels in AD brains suggesting possible contribution of unrepaired DSB to AD development. However, normal aging brains also show reduced DNA-PKcs and Ku levels thus challenging the notion of any direct link between NHEJ and AD. Another kinase, p38 MAPK is induced by various DNA damaging agents and DSB itself. Increased DNA damage with aging could induce p38 MAPK and its induction may be sustained when DNA repair is compromised in the brain with reduced DNA-PK activity. Combined, these two events may potentially set the stage for an awry nervous system approaching AD.
阿尔茨海默病（AD）以神经元普遍死亡和细胞外淀粉样蛋白斑块沉积为特征，其发病机制尚不清楚。据报道，在阿尔茨海默病患者的大脑中，DNA修复能力下降会导致下游DNA病变。神经元主要利用非同源末端连接（NHEJ）机制来修复双链DNA断裂（DSB）。NHEJ需要DNA依赖性蛋白激酶（DNA-PK）的活性。DNA-PK 是一种全酶，由 p460 kD 催化亚基（DNA-PKcs）及其激活剂 Ku（p86 和 p70 亚基的异源二聚体）组成。在 NHEJ 过程开始之前，Ku 首先与 DNA-PKcs 结合，然后将其招募到双链 DNA 末端。研究显示，AD 大脑中的 NHEJ 活性以及 DNA-PKcs 和 Ku 蛋白水平降低，表明未修复的 DSB 可能是导致 AD 发生的原因之一。然而，正常衰老的大脑也显示出DNA-PKcs和Ku水平的降低，从而对NHEJ与AD之间存在任何直接联系的观点提出了质疑。另一种激酶 p38 MAPK 会被各种 DNA 损伤剂和 DSB 本身诱导。随着衰老而增加的DNA损伤可能会诱导p38 MAPK，而当大脑中的DNA修复功能受到损害，DNA-PK活性降低时，p38 MAPK的诱导作用可能会持续。这两个事件结合在一起，有可能为临近 AD 的神经系统失调埋下伏笔。
{"title":"DNA-PK and P38 MAPK: A Kinase Collusion in Alzheimer's Disease?","authors":"Jyotshna Kanungo","doi":"10.4172/2168-975X.1000232","DOIUrl":"10.4172/2168-975X.1000232","url":null,"abstract":"<p><p>The pathogenesis of Alzheimer's disease (AD), characterized by prevalent neuronal death and extracellular deposit of amyloid plaques, is poorly understood. DNA lesions downstream of reduced DNA repair ability have been reported in AD brains. Neurons predominantly use a mechanism to repair double-strand DNA breaks (DSB), which is non-homologous end joining (NHEJ). NHEJ requires DNA-dependent protein kinase (DNA-PK) activity. DNA-PK is a holoenzyme comprising the p460 kD catalytic subunit (DNA-PK<sub>cs</sub>) and its activator Ku, a heterodimer of p86 and p70 subunits. Ku first binds and then recruits DNA-PK<sub>cs</sub> to double-stranded DNA ends before NHEJ process begins. Studies have shown reduced NHEJ activity as well as DNA-PK<sub>cs</sub> and Ku protein levels in AD brains suggesting possible contribution of unrepaired DSB to AD development. However, normal aging brains also show reduced DNA-PK<sub>cs</sub> and Ku levels thus challenging the notion of any direct link between NHEJ and AD. Another kinase, p38 MAPK is induced by various DNA damaging agents and DSB itself. Increased DNA damage with aging could induce p38 MAPK and its induction may be sustained when DNA repair is compromised in the brain with reduced DNA-PK activity. Combined, these two events may potentially set the stage for an awry nervous system approaching AD.</p>","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5504707/pdf/nihms872957.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35167652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01DOI: 10.4172/2168-975X.1000240
A. Ali, M. Khalil, Hemat A. Elariny, Karema Abu-Elfotuh
Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder; lifestyle changes may slow its onset. Mental and physical activities have been related to better cognitive function in older adults. Cognitive engagement and physical activities have been associated with decreased risk of AD. Social isolation refers to a complete absence of or insufficient contact with other members of society and can exacerbate memory deficits. Objective: To study the influence of mental and physical activities in normal socialized conditions as well as to evaluate their role in social isolated conditions on normal and AD rat models. Methods: Rats were divided into two main groups; Group I socialized and Group II isolated. Both socialized and isolated groups were subdivided into four subgroups; two received saline and served as control, while two served as AD subgroups and received ALCl3 (70 mg/kg IP) every day for four weeks. One of the control and AD subgroups was exposed to mental and physical activities but the other not exposed. Mental and physical activities were performed using Swimming test and Y-maze (each for one time/week) during four weeks. Isolated rats were housed individually in cages covered with black plastic while socialized rats randomly paired and housed in transparent covered cages. Histopathological changes in different brain regions and biochemical changes in Aβ, ACHE, brain monoamins (DA, NE, 5-HT), inflammatory mediators (TNF-α, IL-1β), oxidative parameters; (MDA, SOD, TAC) as well as brain derived neurotrophic factor (BDNF) were also measured for all groups. Results: Brain neurological damage characterizing isolation was more pronounced in isolation-associated AD rats. Mental and physical activities significantly decreased Aβ, ACHE, MDA, TNF-α, IL-1β together with increased SOD, TAC, DA, NE, 5-HT and BDNF. The protective effect of mental and physical activities against brain neuronal degenerations was more marked in isolated rats especially in isolated-associated AD rats. These results were confirmed by histopathological examinations of different brain regions. Conclusion: Mental and physical activities can protect from brain neuronal degenerations either induced by isolation or that associated with AD in both socialized and isolated rat models. The protection using mental and physical activities is more pronounced in isolation-associated AD model.
{"title":"The Role of Mental and Physical Activities against Development of Alzheimer′s disease in Socialized and Isolated Rats","authors":"A. Ali, M. Khalil, Hemat A. Elariny, Karema Abu-Elfotuh","doi":"10.4172/2168-975X.1000240","DOIUrl":"https://doi.org/10.4172/2168-975X.1000240","url":null,"abstract":"Background: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder; lifestyle changes may slow its onset. Mental and physical activities have been related to better cognitive function in older adults. Cognitive engagement and physical activities have been associated with decreased risk of AD. Social isolation refers to a complete absence of or insufficient contact with other members of society and can exacerbate memory deficits. Objective: To study the influence of mental and physical activities in normal socialized conditions as well as to evaluate their role in social isolated conditions on normal and AD rat models. Methods: Rats were divided into two main groups; Group I socialized and Group II isolated. Both socialized and isolated groups were subdivided into four subgroups; two received saline and served as control, while two served as AD subgroups and received ALCl3 (70 mg/kg IP) every day for four weeks. One of the control and AD subgroups was exposed to mental and physical activities but the other not exposed. Mental and physical activities were performed using Swimming test and Y-maze (each for one time/week) during four weeks. Isolated rats were housed individually in cages covered with black plastic while socialized rats randomly paired and housed in transparent covered cages. Histopathological changes in different brain regions and biochemical changes in Aβ, ACHE, brain monoamins (DA, NE, 5-HT), inflammatory mediators (TNF-α, IL-1β), oxidative parameters; (MDA, SOD, TAC) as well as brain derived neurotrophic factor (BDNF) were also measured for all groups. Results: Brain neurological damage characterizing isolation was more pronounced in isolation-associated AD rats. Mental and physical activities significantly decreased Aβ, ACHE, MDA, TNF-α, IL-1β together with increased SOD, TAC, DA, NE, 5-HT and BDNF. The protective effect of mental and physical activities against brain neuronal degenerations was more marked in isolated rats especially in isolated-associated AD rats. These results were confirmed by histopathological examinations of different brain regions. Conclusion: Mental and physical activities can protect from brain neuronal degenerations either induced by isolation or that associated with AD in both socialized and isolated rat models. The protection using mental and physical activities is more pronounced in isolation-associated AD model.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86329006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-29DOI: 10.4172/2168-975X.1000226
Tae Yeon Kim, K. Niimi, Eiki Takahashi
Voltage-gated Ca2+ channels (VGCCs) play a pivotal role in intracellular processes such as neurotransmitter release, axonal outgrowth, membrane excitability, and synaptic plasticity. Three major presynaptic Cav2 channels, including the Cav2.1 channel, are involved in the mechanism underlying Ca2+-dependent excitotoxicity. Glutamate is among the excitatory neurotransmitters regulated by the Cav2.1 channel. Glutamate-related excitotoxicity is a pathological process associated with seizures, traumatic brain injury, and cerebral ischemia. This review emphasizes the relationship between activation of the Cav2.1 channel and these various types of brain injury.
{"title":"Role of Cav2.1 Channel Signaling in Glutamate-Related Brain Injury","authors":"Tae Yeon Kim, K. Niimi, Eiki Takahashi","doi":"10.4172/2168-975X.1000226","DOIUrl":"https://doi.org/10.4172/2168-975X.1000226","url":null,"abstract":"Voltage-gated Ca2+ channels (VGCCs) play a pivotal role in intracellular processes such as neurotransmitter release, axonal outgrowth, membrane excitability, and synaptic plasticity. Three major presynaptic Cav2 channels, including the Cav2.1 channel, are involved in the mechanism underlying Ca2+-dependent excitotoxicity. Glutamate is among the excitatory neurotransmitters regulated by the Cav2.1 channel. Glutamate-related excitotoxicity is a pathological process associated with seizures, traumatic brain injury, and cerebral ischemia. This review emphasizes the relationship between activation of the Cav2.1 channel and these various types of brain injury.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73354287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-11-23DOI: 10.4172/2168-975X.1000225
K. Hori, Misa Hosoi, Kimiko Konishi, M. Hachisu, H. Tomioka, Michiho Sodenaga, Chiaki Hashimoto, Ouga Sasaki, Mioto Maedomari, Itsuku Suzuki, Masanori Tadokoro, Sachiko Tsukahara, Hiroyuki Kamatani, Masayuki Tani, Hiroaki Tanaka, Y. Kitajima, H. Kocha
In this article, we reviewed our previous articles those showed that ageing process and disease progression connected affective disturbances and anxiety with delusion, hallucination and aggressiveness and those behavioral and psychological symptoms of dementia (BPSD) is related with bipolarity (BT), and we comment the pharmacotherapies for BPSD in Alzheimer’s disease (AD). There are two types of BPSD with AD. One is related with the progressions of AD that is caused by the deteriorated lesions by AD pathology. Therefore, these symptoms are ameliorated by the treatment for AD, that is, cholinesterase inhibitors or N-methyl-D-aspartate receptors antagonist. The other is related with brain reserve (BR) and cognitive reserve (CR). In this pattern, the information processing system is not deteriorated. However, low BR caused by BT and low CR modulate the behaviors etwas eccentric. When lowering of brain volume caused by AD pathology is added, i.e., BR is lower than before, BPSD appears. Therefore, in this patter, SSRI, atypical antipsychotics and anticonvulsants those have the treatment option for bipolar disorders, galanatmine and SNRI are needed.
在本文中，我们回顾了前人关于衰老过程和疾病进展将情感障碍和焦虑与妄想、幻觉和攻击性联系起来的研究，以及老年痴呆症(BPSD)的行为和心理症状与双极性(BT)有关的研究，并对BPSD在老年痴呆症(AD)中的药物治疗进行了评述。有两种类型的BPSD与AD。一种与阿尔茨海默病的进展有关，这是由阿尔茨海默病病理引起的病变恶化引起的。因此，通过治疗AD，即胆碱酯酶抑制剂或n -甲基- d -天冬氨酸受体拮抗剂，这些症状得到改善。另一个与脑储备(BR)和认知储备(CR)有关。在这种模式下，信息处理系统不会恶化。然而，由BT和低CR引起的低BR对行为的调节是偏心的。当加上AD病理导致的脑容量降低，即脑容量比术前降低时，出现BPSD。因此，在这种情况下，需要使用SSRI、非典型抗精神病药和抗惊厥药(双相情感障碍的治疗选择)、galanatamine和SNRI。
{"title":"Pharmacotherapies for Behavioral and Psychological Symptomsof Dementia with AlzheimerâÂÂs Disease: Two Subcategories of theseSymptoms","authors":"K. Hori, Misa Hosoi, Kimiko Konishi, M. Hachisu, H. Tomioka, Michiho Sodenaga, Chiaki Hashimoto, Ouga Sasaki, Mioto Maedomari, Itsuku Suzuki, Masanori Tadokoro, Sachiko Tsukahara, Hiroyuki Kamatani, Masayuki Tani, Hiroaki Tanaka, Y. Kitajima, H. Kocha","doi":"10.4172/2168-975X.1000225","DOIUrl":"https://doi.org/10.4172/2168-975X.1000225","url":null,"abstract":"In this article, we reviewed our previous articles those showed that ageing process and disease progression connected affective disturbances and anxiety with delusion, hallucination and aggressiveness and those behavioral and psychological symptoms of dementia (BPSD) is related with bipolarity (BT), and we comment the pharmacotherapies for BPSD in Alzheimer’s disease (AD). There are two types of BPSD with AD. One is related with the progressions of AD that is caused by the deteriorated lesions by AD pathology. Therefore, these symptoms are ameliorated by the treatment for AD, that is, cholinesterase inhibitors or N-methyl-D-aspartate receptors antagonist. The other is related with brain reserve (BR) and cognitive reserve (CR). In this pattern, the information processing system is not deteriorated. However, low BR caused by BT and low CR modulate the behaviors etwas eccentric. When lowering of brain volume caused by AD pathology is added, i.e., BR is lower than before, BPSD appears. Therefore, in this patter, SSRI, atypical antipsychotics and anticonvulsants those have the treatment option for bipolar disorders, galanatmine and SNRI are needed.","PeriodicalId":9146,"journal":{"name":"Brain disorders & therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2016-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91466103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-10-15DOI: 10.4172/2168-975X.1000224
Tomohiro Ikeda, K. Hori, Atsuko Inamoto, Takuro Nakatsubo, J. Koike, Satoru Sugisawa, T. Tsuneoka, M. Mimura, A. Iwanami
Background: Although psychoeducational programs for patients with schizophrenia have become relatively standardized, the correlation between effectiveness of such programs and cognitive function has rarely been investigated. To the best of our knowledge, studies detailing the effectiveness of such programs on cognitive function in Japan have yet to be reported. Method: Participants included 91 patients with schizophrenia (women, n=46; men, n=45; mean age, 43.2 years) who had been admitted to a subacute care unit in Showa University Karasuyama Hospital and who had given their consent to participate. In this study, a new psychoeducation-based, psychosocial intervention program (the Program) was initiated. The effectiveness of the Program was evaluated by the comparisons with global daily function and daily cognitive functions between pre and post intervention in patients. Results and discussion: Our results showed that the global assessment of functioning (GAF) score was significantly associated with the Wisconsin card sorting test (WCST) total number of errors and perseverative errors. We confirmed that the effectiveness of the Program and global functional improvement is related with improvement of executive function.Conclusion: On the basis of these results, future studies are warranted to improve our program and confirm its long-term effectiveness.
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